Adipose‐derived factor CTRP9 attenuates vascular smooth muscle cell proliferation and neointimal formation
| العنوان: | Adipose‐derived factor CTRP9 attenuates vascular smooth muscle cell proliferation and neointimal formation |
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| المؤلفون: | Yusuke Uemura, Yasuhiro Ogura, Yusuke Joki, Noriyuki Ouchi, Koji Ohashi, Toyoaki Murohara, Takashi Yamamoto, Rei Shibata, Megumi Miyabe, Kazuhiro Matsuo, Takashi Enomoto, Takahiro Kambara, Daisuke Yuasa, Yoshiyuki Kataoka |
| المصدر: | The FASEB Journal. 27:25-33 |
| بيانات النشر: | Wiley, 2012. |
| سنة النشر: | 2012 |
| مصطلحات موضوعية: | Male, MAPK/ERK pathway, medicine.medical_specialty, Vascular smooth muscle, medicine.medical_treatment, Blotting, Western, Adipose tissue, Biochemistry, Muscle, Smooth, Vascular, Mice, Restenosis, Internal medicine, Genetics, Animals, Humans, Medicine, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Molecular Biology, Cells, Cultured, Cell Proliferation, Glycoproteins, Neointimal hyperplasia, biology, business.industry, Cell growth, Growth factor, Anatomy, medicine.disease, Recombinant Proteins, Tumor Necrosis Factor Receptor-Associated Peptides and Proteins, Mice, Inbred C57BL, Endocrinology, Adipose Tissue, biology.protein, Adiponectin, Tunica Intima, business, Platelet-derived growth factor receptor, Biotechnology |
| الوصف: | Obesity is closely associated with the progression of vascular disorders, including atherosclerosis and postangioplasty restenosis. C1q/TNF-related protein (CTRP) 9 is an adipocytokine that is down-regulated in obese mice. Here we investigated whether CTRP9 modulates neointimal hyperplasia and vascular smooth muscle cell (VSMC) proliferation in vivo and in vitro. Left femoral arteries of wild-type (WT) mice were injured by a steel wire. An adenoviral vector expressing CTRP9 (Ad-CTRP9) or β-galactosidase as a control was intravenously injected into WT mice 3 d before vascular injury. Delivery of Ad-CTRP9 significantly attenuated the neointimal thickening and the number of bromodeoxyuridine-positive proliferating cells in the injured arteries compared with that of control. Treatment of VSMCs with CTRP9 protein attenuated the proliferative and chemotactic activities induced by growth factors including platelet-derived growth factor (PDGF)-BB, and suppressed PDGF-BB-stimulated phosphorylation of ERK. CTRP9 treatment dose-dependently increased cAMP levels in VSMCs. Blockade of cAMP-PKA pathway reversed the inhibitory effect of CTRP9 on DNA synthesis and ERK phosphorylation in response to PDGF-BB. The present data indicate that CTRP9 functions to attenuate neointimal formation following vascular injury through its ability to inhibit VSMC growth via cAMP-dependent mechanism, suggesting that the therapeutic approaches to enhance CTRP9 production could be valuable for prevention of vascular restenosis after angioplasty. |
| تدمد: | 1530-6860 0892-6638 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fdc8c7ce63ba720232e29860fdd3df58Test https://doi.org/10.1096/fj.12-213744Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....fdc8c7ce63ba720232e29860fdd3df58 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15306860 08926638 |
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